Pharmacological challenge and synaptic response - assessing dopaminergic function in the rat striatum with small animal single-photon emission computed tomography (SPECT) and positron emission tomography (PET).

摘要: Disturbances of dopaminergic neurotransmission may be caused by changes in concentrations synaptic dopamine (DA) and/or availabilities pre- and post-synaptic transporter receptor binding sites. We present a series experiments which focus on the regulatory mechanisms dopamin(DA)ergic synapse rat striatum. In these studies, DA (DAT) D(2) were assessed with either small animal single-photon emission computed tomography (SPECT) or positron (PET) after pharmacological challenge haloperidol, L-DOPA methylphenidate, nigrostriatal 6-hydroxydopamine lesion. Investigations DAT performed [(123)I]N-ω-fluoropropyl-2β-carbomethoxy-3β-(4-iodophenyl)nortropane ([(123)I]FP-CIT). bindingd was [(123)I](S)-2-hydroxy-3-iodo-6-methoxy-N-[(1-ethyl-2-pyrrolidinyl)methyl]benzamide ([(123)I]IBZM) [(18)F]1[3-(4'fluorobenzoyl)propyl]-4-(2-keto-3-methyl-1-benzimidazolinyl)piperidine ([(18)F]FMB). Findings demonstrate that vivo investigations are feasible SPECT PET. Therefore, tracers radiolabeled isotopes comparatively long half-lives such as (123)I employed. Our approach to quantify at baseline interventions inducing blockade, increases decreases endogenous holds promise for assessment function. This pertains models diseases associated postsynaptic DAergic deficiencies Parkinson's disease, Huntington's attention-deficit/hyperactivity disorder, schizophrenia drug abuse.